NRS 3026 Chapter 19 Normal Newborn Processes of Adaptation

what expands the alveoli and is essential for the development of fetal lungs?

surfactant

benefits of surfactant

reduces surface tension within alveoli

sufficient by 34-36 weeks of gestation

what is given to a mom in preterm labor to help increase surfactant production and speed lung maturation?

betamethasone

in the carotid arteries, what responds to changes in blood chemistry caused by the hypoxemia that occurs with normal birth?

chemoreceptors

this is d/t compression of the vaginal canal and cord

what stimulates the respiratory center in the medulla?

decrease in partial pressure of O2 and pH + increase in partial pressure of CO2 in the blood

During vaginal birth, how is negative pressure reduced (which is needed for the first breath after birth)?

pressure against the chest during movement through the vaginal canal is released

this causes a recoil of the chest thus drawing in a small amount of air into the lungs

this helps remove some viscous fluid too

other factors that help stimulate initiation of respirations

skin sensors respond to temperature change and send an impulse to the medulla to stimulate the respiratory center and breathing

stimulation of light, sound, smell, pain

why/how do the alveoli remain partially expanded/open between respirations?

surfactant keeps them open because open alveoli allows subsequent breaths to require less effort

as the baby cries, pressure in the lungs increase causing fetal lung fluid to move into interstitial spaces

internal respiration stimuli

decreased PO2, pH & increased PCO2 → message to respiratory center in medulla → diaphragm is stimulated to contract → first breath drawn

external stimuli for respirations

chest compression and release during birth thru canal → cold air and touch stimulate skin sensors → skin impulses and responses to sound/light affect respiratory center → first breath

cardiovascular adaptation at birth

pressure between R/L sides of the heart in the first few minutes are reversed

shunts close, pulmonary vessels dilate

foramen ovale’s flap valve closes

clamping of umbilical cord closes ductus venosus

heat loss methods: convection

flow of heat from body surface to cooler surrounding air

ex: air conditioner, draft cause heat loss by convention

prevent: wrap baby in warm blanket and keep room at 70-72F

heat loss methods: radiation

transfer of heat to cooler objects or surfaces not in contact with the body

ex: cold window surfaces, examining tables near baby

prevent: move baby away from cold objects

heat loss methods: evaporation

loss of heat due to conversion of liquid to vapor

ex: wet newborns lose a great amount of heat when the amniotic fluid in the skin evaporates (heat loss after birth is mainly from this)

prevent: wipe newborn dry immediately to prevent heat loss

heat loss methods: conduction

loss of heat by way of cooler surfaces in contact with the body

ex: when a newborn is placed on a cold scale, counter, or crib

prevention: warm objects that are placed directly on newborns

thermoregulation behaviors

newborns do not shiver (unless prolonged exposure) when they are cold

sx: restless, cry, increased activity/flexion, peripheral vasoconstriction, increase in metabolic rate cause above normal oxygen and glucose use, hypoglycemia

non-shivering thermogenesis (NST)

brown fat (fat with abundant supply of BV around the back of the neck, axillae, around the heart, kidneys, adrenals, between scapulae, and abdominal aorta) is metabolized to generate heat

blood passes through the brown fat → warm blood → carried throughout the body

metabolized with oxygen and glucose

cold stress

prolonged periods of hypothermia and can deplete brown fat stores → ultimately increases risk for permanent brain damage/death

causes of cold stress: increased metabolic rate

hypoglycemia, increase RR, respiratory distress → depression, diminished production of surfactant

causes of cold stress: metabolism of brown fat

increases fatty acid production → metabolic acidosis → interferes with bilirubin transport → hyperbilirubinemia

causes of cold stress: vasoconstriction

in an attempt to retain heat, peripheral vessels cause pale/cold/mottled skin → permanent brain damage or death → PICU

what is necessary to activate clotting factors (FII, VII, IX, X)?

vitamin K

where is vitamin K synthesized?

in the intestines, but food and normal intestinal flora are necessary for this process

newborns have sterile intestines → no vitamin K production

newborn platelet ranges first born vs after 1 week

84-478k at birth (lacks response to stimuli)

150-400k 1 week

blood glucose maintainance in the fetus

glucose is supplied by the placenta and is stored as glycogen in during the third trimester

what does the baby use as energy when feeding has not been established yet?

glycogen stores

uses: energy during delivery stress, breathing, heat production, movement against gravity

how long does it take for glycogen stores to deplete after birth?

12hrs

are all newborns at risk for hypoglycemia?

yes

normal glucose levels for full-term baby?

1st day of life: 40-60 mg/dL

thereafter: 50-90mg/dL

hypoglycemia newborn range

<40-45mg/dL

risk factors for hypoglycemia

1. pre-term/late preterm/ small for gestational age (SGA) → bc low glycogen stores

2. post-term infant → bc decreased transfer through placenta

3. large for gestational age (LGA), diabetic moms → hyperinsulinemia

   1. infants exposed to stressors → asphyxia, infxn, cold stress

hypoglycemia sx

jitteriness, poor muscle tone, diaphoresis, poor suck, tachypnea, tachycardia, dyspnea, grunting, cyanosis, apnea, low temp, high-pitched cry, irritable, lethargy, seizure, coma

rigid → flaccid is really bad

newborn GI system

capacity expands within first few days of life

rapid peristalsis

gastrocolic reflex is stimulated when the stomach fills

cardiac sphincter is relaxed → regurgitation

is breastmilk or formula faster to digest?

breastmilk is 2x faster

newborn intestines

long in proportion to infant’s size therefore more SA to absorb

more prone to rapid water loss with diarrhea

bowel sounds present within first hour

digestive tract is sterile until feeding begins

what do infants have a hard time digesting?

complex carbohydrates in formula → more spit

saliva production is limited until what month of life?

3 months

meconium color and characteristics

first stool excreted: green-black with a thick, sticky, tar-like consistency

passed within first 24hrs and has particles of amniotic fluid

what is the second type of stool?

transitional stool (combination of meconium and milk stools)

breastfed infant stools

seedy, mustard color, sweet-sour smell

more frequent

formula fed infant stools

pale yellow-light brown, stool-like odor

firmer in consistency

stool frequency

Day 1: 1 pee and 1 poo

Hours 24-48: 2 pee and 2 poo

Hours 48-72: 3 pee and 3 poo

what organ conjugates bilirubin?

liver

is the newborn’s liver mature to prevent hyperbilirubinemia (jaundice) during the first week of life?

no

bilirubin source and effects

source: hemolyzed RBCs

effect: toxic, liver converts it to a soluble/conjugated form which is excreted in the stool, unconjugated bilirubin leads to jaundice and kernicterus (brain damage)

what increases bilirubin?

excessive hemolysis, short RBC lifespan, liver immaturity, insufficient breastfeeding, blood incompatibility, preterm or late-term, trauma causing bruising or cephalhematoma, polycythemia, jaundiced sibiling, males, asia, AA, native american, maternal diabetes, preeclampsia

physiologic jaundice

due to transient hyperbilirubinemia and never present during first 24hrs of life

usually peaks around 3 days of life (monitor rise and falls in bilirubin)

what level of bilirubin is jaundice noticable?

bilirubin >5mg/dL

non-physiologic (pathologic) jaundice

occurs in first 24hrs of life from excessive destruction of RBC or bilirubin conjugation issues

scarier

breastfeeding jaundice

due to inadequate intake, sleepy infant with poor suck, delayed elimination of meconium

true breast milk jaundice

bilirubin levels rise after first 3-5 days because substances in the milk interfere with bilirubin conjugation

tx: phototherapy and discontinue breastfeeding

phototherapy

bilirubin in the skin absorbs the light and changes into water-soluble products that are excreted in bile and urine

2 types of phototherapy

1. bili-lights: bank of fluorescent lamps

2. bili-blanket: portable fiber-optic pad and illuminator

phototherapy RN care

protect eyes and genitals, hydration, encourage bonding

differentiate physiologic and pathologic jaundice

physiologic: jaundice appears on day 2-3 from an immature liver, no tx bc its normal

pathologic: jaundice appears before first 24hrs from excess hemolysis, incompatibility, infxn, metabolic disorder, tx phototherapy

is a newborn’s kidney function mature?

no it is immature

urinary system of newborn

<24hrs: void once

24-48hrs: 2 voids

48-72hrs: 3-4 voids

Day 4: at least 6-8 within 24 hours because feedings are established and milk is mature

passive/acquired immunity

received in 3rd trimester and in breastmilk

gradually disappears with lowest levels at 2-4 months

IgG crosses placenta in 3rd trimester

Secretory IgA received in colostrum and breast milk

active / produced immunity

first immunity produced by the newborn

IgM: used for GN bacteria

IgA: protects GI and respiratory systems

A first time father is concerned that his 3 day old daught'er’s skin looks yellow. in the nurse’s explanation of physiologic jaundice, which point should be included?

physiologic jaundice occurs during the first 24hrs of life

physiologic jaundice is caused by blood incompatibilities between the mother and infant blood types

bilirubin levels of physiologic jaundice peak at 5-7 mg/dL between 2-4th day of life

this condition is breast milk jaundice

bilirubin levels of physiologic jaundice peak at 5-7 mg/dL between 2-4th day of life